Calcium oscillations triggered by cardiotonic steroids

Na⁺, K⁺–ATPase (NKA) is well known for its function as an ion pump. Studies during the last decade have revealed an additional role for NKA as a signal transducer. In this brief review, we describe how cardiotonic steroids, which are highly specific NKA ligands, trigger slow Ca²⁺ oscillations by promoting the interaction between NKA and the inositol trisphosphate receptor, and how this Ca²⁺ signal activates the NF‐κB subunit p65 and increases the expression of the antiapoptotic factor Bcl‐xL. The potential tissue‐protective effects of this signal are discussed.